In recent years, dementia has become a significant medical problem worldwide. Dementia is a disease associated with various symptoms mainly including learning and memory disorders and impaired judgment, in which the symptoms and progression thereof vary depending on the causative diseases thereof. In any case, they are common in that they markedly impair the quality of life of the patients. In consideration of the fact that dementia forces huge labor to the caregivers including patients' families, it is a very serious social problem. It is predicted that the dementia patients will further increase hereafter in Japan, since an increase in the population of elderly people due to prolongation of life span is related to an increase in the dementia patients. In addition, there are many people suffering from cognitive impairment due to aging, which is not classified as dementia.
Various compounds capable of improving dementia have been reported. 8-[2-(2-Pentyl-cyclopropylmethyl)-cyclopropyl]-octanoic acid (DCP-LA), which is a linoleic acid derivative, is a compound having a long-term enhancing action on synapse transmission efficiency, which can delay metabolism in the body and can maintain stable LTP (long-term potentiation)-like enhancement of synapse transmission (patent document 1). LTP is considered to be involved in the improvement of, for example, various neurological and mental diseases such as Alzheimer's disease and the like, and therefore, a substance that induces LTP expression has a possibility of providing a therapeutic or prophylactic drug for these neurological and mental diseases including dementia.
Some reports have also been documented as regards DCP-LA. For example, it has been reported that DCP-LA activates PKC-ε selectively and directly (non-patent document 1), DCP-LA improves cognitive dysfunction of senescence accelerated mouse (non-patent document 2), DCP-LA increases release of γ aminobutyric acid from hippocampus nerve cells (non-patent document 3), DCP-LA improves cognitive dysfunction of amyloid β peptide or scopolamine-treated rat (non-patent document 4), and DCP-LA promotes hippocampal synaptic transmission with α7 nicotinic acetylcholine receptor expressed in glutamatergic presynaptic cell as a target (non-patent document 5). Furthermore, it has been reported in recent years that DCP-LA has an action to suppress nerve cell death induced by oxidative stress (patent document 2).
However, a detailed mechanism of the synaptic transmission promoting action of DCP-LA has not been elucidated yet. Elucidation of the mechanism to clarify the point of action of DCP-LA leads to the development of a prophylactic or therapeutic drug for various neurodegenerative diseases including Alzheimer's disease, which has an action mechanism different from that of existing drugs.